Horner Syndrome: Overview, Anatomy, Pathophysiology 7/19/17, 6:45 AM

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Horner Syndrome
Updated: May 17, 2016
Author: Christopher M Bardorf, MD, MS; Chief Editor: Edsel Ing, MD, MPH, FRCSC more...

OVERVIEW

Overview
Horner syndrome (Horner’s syndrome) results from an interruption of the sympathetic nerve
supply to the eye and is characterized by the classic triad of miosis (ie, constricted pupil), partial
ptosis, and loss of hemifacial sweating (ie, anhidrosis). The term Horner syndrome is commonly
used in English-speaking countries, whereas the term Bernard-Horner syndrome is common in
France. Von Passow syndrome is an association of Horner syndrome with iris heterochromia
(heterochromia iridis). [1]

Causes of Horner syndrome include the following:

Lesion of the primary neuron

Brainstem stroke or tumor or syrinx of the preganglionic neuron – In one study, 33% of
patients with brainstem lesions demonstrated Horner syndrome [2]
Trauma to the brachial plexus
Tumors (eg, Pancoast) or infection of the lung apex
Lesion of the postganglionic neuron
Dissecting carotid aneurysm – In one study, 44% (65/146) of patients with internal
extracranial carotid artery dissections had painful Horner syndrome, which remained
isolated in half the cases (32/65) [3]
Carotid artery ischemia
Migraine
Middle cranial fossa neoplasm

Horner syndrome is uncommon. No age, sexual, or racial predilections are known to exist. The
prognosis and the complications to be expected depend on the underlying cause of the
syndrome, as does treatment.

Anatomy
Sympathetic innervation to the eye consists of a 3-neuron arc. First-order central sympathetic
fibers arise from the posterolateral hypothalamus, descend uncrossed through the midbrain and
pons, and terminate in the intermediolateral cell column of the spinal cord at the level of C8-T2
(ciliospinal center of Budge). Second-order preganglionic pupillomotor fibers exit the spinal cord
at the level of T1 and enter the cervical sympathetic chain, where they are in close proximity to
the pulmonary apex and the subclavian artery.

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The fibers ascend through the sympathetic chain and synapse in the superior cervical ganglion
at the level of the bifurcation of the common carotid artery (C3-C4). Postganglionic pupillomotor
fibers exit the superior cervical ganglion and ascend along the internal carotid artery. Shortly
after the postganglionic fibers leave the superior cervical ganglion, vasomotor and sudomotor
fibers branch off, traveling along the external carotid artery to innervate the blood vessels and
sweat glands of the face.

The third-order pupillomotor fibers ascending along the internal carotid artery enter the
cavernous sinus. The fibers then leave the carotid plexus briefly to join the abducens nerve
(cranial nerve [CN] VI) in the cavernous sinus and enter the orbit through the superior orbital
fissure along with the ophthalmic branch (V1) of the trigeminal nerve (CN V) via the long ciliary
nerves. The long ciliary nerves then innervate the iris dilator and the Müller muscle.

Pathophysiology
Horner syndrome may develop from lesions at any point along the sympathetic pathway. [4]
Abnormalities found in all patients, regardless of the level of interruption, include the following:

Mild-to-moderate ptosis, owing to denervation of the sympathetically controlled Müller

muscle
Slight elevation of the lower lid (upside-down ptosis), owing to denervation of the lower lid
muscle (analogous to the denervation of the Müller muscle in the upper lid)
Miosis and dilation lag, where pupillary dilation after psychosensory stimuli is slower in the
affected pupil than in the unaffected pupil

Depending on the level of the lesion, impaired flushing and sweating may be found ipsilaterally.
With central first-order neuron lesions, anhidrosis affects the ipsilateral side of the body. Lesions
affecting second-order neurons may cause anhidrosis of the ipsilateral face. With postganglionic
lesions occurring after vasomotor and sudomotor fibers have branched off the sympathetic
chain, anhidrosis is either absent or limited to an area above the ipsilateral brow. The pupils
react normally to light and accommodation.

Iris heterochromia (with the affected eye being hypopigmented) is seen in congenital Horner
syndrome or Horner syndrome that occurs in children younger than 2 years. Iris heterochromia
also may occur in long-standing Horner syndrome.

Etiology
Horner syndrome can be congenital, acquired, or purely hereditary (autosomal dominant). The
interruption of the sympathetic fibers may occur centrally (ie, between the hypothalamus and the
fibers’ point of exit from the spinal cord [C8 to T2]) or peripherally (ie, in cervical sympathetic
chain, at the superior cervical ganglion, or along the carotid artery). [5]

The common lesions that cause Horner syndrome interfere with preganglionic fibers as they
course through the upper thorax. Virtually all lesions producing postganglionic sympathetic
dysfunction are located intracranially or intraorbitally because the superior cervical ganglion is
near the skull. Preganglionic Horner syndrome indicates a serious underlying pathology and is
associated with a high incidence of malignancy. Postganglionic involvement has primarily benign
causes (ie, usually a vascular headache).

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Causes of Horner syndrome may also be classified as involving first-order, second-order, or

third-order neuron lesions. First-order neuron lesions that may give rise to the syndrome include
the following:

Arnold-Chiari malformation
Basal meningitis (eg, syphilis)
Basal skull tumors
Cerebral vascular accident (CVA)/Wallenberg syndrome (lateral medullary syndrome)
Demyelinating disease (eg, multiple sclerosis)
Lesions in the hypothalamus or medulla
Intrapontine hemorrhage
Neck trauma (eg, traumatic dislocation of cervical vertebrae or traumatic dissection of the
vertebral artery) - Horner syndrome occurring in association with spinal cord trauma
suggests a high cervical cord lesion because it does not occur with lesions below T2 or T3
Pituitary tumor
Syringomyelia

Second-order neuron lesions that may give rise to Horner syndrome include the following:

Pancoast tumor (tumor in the apex of the lung, most commonly squamous cell carcinoma)
Birth trauma with injury to lower brachial plexus [6]
Cervical rib
Aneurysm or dissection of the aorta
Lesions of the subclavian or common carotid artery
Central venous catheterization
Trauma or surgical injury (eg, due to radical neck dissection, thyroidectomy, [7] carotid
angiography, radiofrequency tonsil ablation, [8] chiropractic manipulation, [9] or coronary
artery bypass grafting)
Chest tubes
Lymphadenopathy (eg, Hodgkin disease, leukemia, tuberculosis, or mediastinal tumors)
Mandibular tooth abscess
Lesions of the middle ear (eg, acute otitis media)
Neuroblastoma [10]

Third-order neuron lesions that may give rise to Horner syndrome include the following:

Internal carotid artery dissection (associated with sudden ipsilateral face or neck pain) [11]
Raeder syndrome (paratrigeminal syndrome) - Oculosympathetic paresis and ipsilateral
facial pain with variable involvement of the trigeminal and oculomotor nerves
Carotid cavernous fistula
Cluster or migraine headache
Herpes zoster

Clinical Presentation
Patient history

Obtaining a careful history is very helpful in the localization of lesions causing Horner syndrome.
The symptoms reported by the patient will depend on the underlying cause, as follows:

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First-order neuron lesions – Hemisensory loss, dysarthria, dysphagia, ataxia, vertigo, and
nystagmus
Second-order neuron lesions – Prior trauma; facial, neck, axillary, shoulder or arm pain;
cough; hemoptysis; previous thoracic or neck surgery; previous chest tube or central
venous catheter placement; or neck swelling
Third-order neuron lesions – Diplopia from sixth nerve palsy, numbness in the distribution
of the first or second division of the trigeminal nerve (cranial nerve [CN] V), and pain

Although Horner syndrome is commonly an incidental finding related to a benign cause, it

occasionally may be a manifestation of a serious and life-threatening disorder. Careful direction
of the history to rule out such life-threatening disorders is vital.

Given that malignancy is a prominent feature of recently diagnosed preganglionic Horner

syndrome, patients may avoid an unnecessary extensive workup for carcinoma if the lesion can
be shown to be old or long-standing. To prove that a lesion is long-standing, inspect old
photographs of the patient that might show ptosis or anisocoria. If the affected iris is blue and
the other is brown, the lesion most likely was present at birth or during the first 2 years of life.
(Of course, this color asymmetry will not occur in patients who are genetically blue-eyed.)

It is important to determine whether the patient has recently undergone an interventional

procedure that has the potential to cause relevant neurologic damage. Iatrogenic Horner
syndrome has been reported as a complication of a variety of chest, neck, and otolaryngologic
procedures [12, 13, 14, 15, 16] ; for example, ptosis may rarely complicate injection of botulinum
toxin for glabellar lines. [17]

Patients may not be able to open the affected eye completely and may not sweat on that side of
the face. The presence, absence, or location of anhidrosis is an important localizing sign.

Patients with preganglionic lesions may have facial flushing. This symptom (ie, harlequin effect)
occurs with physical exercise in some patients. Patients with postganglionic lesions may have
ipsilateral orbital pain or a migrainelike headache.

Raeder described a combination of orbital pain, miosis, and ptosis and termed it paratrigeminal
syndrome. [18] If this set of symptoms is associated with lesions of CNs III-VI on the ipsilateral
side, a mass lesion in the middle cranial fossa (ie, type I Raeder paratrigeminal syndrome)
should be suspected. A benign form characterized by episodic retrobulbar or orbital pain, with
miosis and ptosis but without associated cranial nerve findings, is considered a migraine variant
(ie, type II Raeder paratrigeminal syndrome).

Patients with carotid artery dissection may present with ipsilateral head, neck, or facial pain.

Physical examination

Important aspects of the physical examination include the following:

Measurement of pupillary diameter in dim and bright light and the reactivity of the pupils to
light and accommodation
Examination for dilation lag of the pupil immediately after the room lights are dimmed
Examination of the upper lids for ptosis
Examination of the lower lids for upside-down ptosis (eg, the position of the lower lid with

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respect to the inferior limbus)

Observation of extraocular movements
Biomicroscopic examination of the pupillary margin and iris structure and color
Confrontational visual field testing and testing of facial sensation
Observation for the presence of nystagmus, facial swelling, lymphadenopathy, or vesicular
eruptions

The pupil on the affected side may be round and constricted (ie, miosis). In individuals with
Horner syndrome, the anisocoria is greater in darkness than in light. The affected pupil dilates
more slowly than the normal pupil does because the affected pupil lacks the pull of the dilator
muscle (ie, dilation lag). Patients may have a loss of the ciliospinal reflex (ie, afferent C2, C3), in
which the pupil fails to dilate when the skin on back of the neck is pinched. (Most authors,
however, consider this finding unreliable.)

Patients have dry skin (ie, anhidrosis) on the same side of their face as the affected pupil. The
pattern of a patient’s inability to sweat may be helpful in localizing the lesion. If a patient has a
lesion in the area of the common carotid artery, loss of sweating involves the entire side of the
face. With lesions distal to the carotid bifurcation, the lack of sweating is confined to the medial
aspect of the forehead and the side of the nose.

Other findings that may be noted include the following:

Partial ptosis
Apparent enophthalmos – Assertions to the contrary notwithstanding, true enophthalmos
does not occur; the ptosis merely gives an illusion created by narrowing of the palpebral
fissure, which results from weakness of the muscle of Müller in both the upper lid (causing
partial ptosis) and the lower lid (causing slight elevation of lower eyelid)
Increased amplitude of accommodation
Iris heterochromia (heterochromia iridis) – The affected iris may remain blue when the
other iris changes to brown; this may be present if the lesion is in a child younger than 2
years but is uncommon in older patients; iris pigmentation is under sympathetic control
during development, which is completed by the age of 2 years
Paradoxical contralateral eyelid retraction
Transient decrease in intraocular pressure and changes in tear viscosity
Absence of a horizontal eyelid fold or crease in the ptotic eye, especially in patients with
congenital Horner syndrome
Red conjunctivae

Differential Diagnosis
Horner syndrome in the presence of pain merits special consideration.

Horner syndrome in the presence of axial, shoulder, scapula, arm, or hand pain may be
indicative of compression by an apical lung tumor (Pancoast tumor).

Horner syndrome in the presence of acute-onset, ipsilateral facial or neck pain may indicate
carotid artery dissection, which may be caused by cardiovascular disease, arteriopathy (eg,
fibromuscular dysplasia or collagen disorders), or trauma (even minor trauma, such as results
from quick head turns). If carotid artery dissection is suspected, especially if there are signs or
symptoms of retinal ischemia, urgent neuroimaging studies (magnetic resonance imaging or

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magnetic resonance angiography) should be obtained along with neurologic consultation.

Postganglionic Horner syndrome associated with ipsilateral headache has several causes.
Patients with spontaneous carotid artery dissection may present with Horner syndrome and
ipsilateral headache. Patients with cluster headaches may develop ipsilateral Horner syndrome
during an acute attack.

The term Raeder paratrigeminal syndrome is applied to patients, usually middle-aged males,
who have Horner syndrome and daily unilateral head pain. In the original Raeder syndrome, the
pain is trigeminal pain associated with hypoesthesia or anesthesia in the distribution of the
trigeminal nerve (cranial nerve [CN] V). Pain related to Raeder syndrome can be distinguished
from that related to cluster headaches or carotid disease in that the latter conditions occur
without impairment of trigeminal nerve function.

Horner syndrome may be the first manifestation of neuroblastoma.

Conditions to be considered in the differential diagnoses include the following:

Adie pupil
Physiologic anisocoria and involutional ptosis
Argyll Robertson pupil
Holmes-Adie pupil (contralateral)
Iris sphincter muscle damage
Senile miosis
Third nerve palsy

Unilateral use of miotic drugs or mydriatic drugs should also be considered in the differential
diagnoses. Other medications to consider include local anesthetics (lidocaine, bupivacaine,
etidocaine), acetophenazine, alseroxylon, butaperazine, carphenazine, chloroprocaine,
chlorpromazine, deserpidine, diacetylmorphine, diethazine, ethopropazine, fluphenazine,
guanethidine, influenza virus vaccine, levodopa, lidocaine, mesoridazine, methdilazine,
methotrimeprazine, oral contraceptives, perazine, prilocaine, procaine, prochlorperazine,
promazine, promethazine, propoxycaine, reserpine, thioproperazine, thioridazine, and
trifluoperazine.

Laboratory Studies
In general, laboratory studies do not play a significant role in the diagnosis and management of
Horner syndrome. However, depending on the localization and suspected etiology, certain
laboratory tests may be considered, as follows:

Urine test (ie, vanillylmandelic acid [VMA] and homovanillic acid [HVA]) in pediatric Horner
syndrome to rule out neuroblastoma
Complete blood count (CBC)
Fluorescent treponemal antibody absorption (FTA-ABS) test
Venereal Disease Research Laboratory (VDRL) test (for rare cases of syphilitic basilar
meningitis or when Argyll Robertson pupil is suspected)
Purified protein derivative (PPD) placement

Imaging Studies
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Imaging studies may be ordered in conjunction with appropriate medical or surgical consultation,
depending on the localization and suspected etiology. [19]

A chest radiograph should be obtained; apical bronchogenic carcinoma is the most common
cause of Horner syndrome. If stroke is suspected, computed tomography (CT) of the head
should be performed.

Painful Horner syndrome should alert the physician to the possibility of carotid artery dissection,
and the patient should undergo further testing (ie, magnetic resonance imaging [MRI]/magnetic
resonance angiography [MRA] of the brain and neck) to exclude this possibility. Internal carotid
artery dissection is life-threatening and carries a risk that the patient will experience a disabling
stroke.

Ultrasonography may be considered but has not been found to be reliable for diagnosing carotid
artery dissection in patients with isolated Horner syndrome. [20]

Pharmacologic Testing
Pharmacologic testing is very helpful in the diagnosis of Horner syndrome. [21] The following
pharmacologic tests document the presence or absence of an ocular sympathetic lesion and
identify the level of involvement (ie, preganglionic or postganglionic). Localizing the lesion is
important because preganglionic lesions are associated with a higher incidence of malignancy
that necessitates extensive investigations.

Topical cocaine test

The basis for the topical cocaine test is the ability of cocaine to act as an indirect
sympathomimetic agent by inhibiting the reuptake of norepinephrine from the synaptic cleft at
the nerve ending.

The test is performed by instilling cocaine solution (2-4% or, according to some, 4-10%) into
each eye. Cocaine instilled in an eye with intact sympathetic innervation causes the pupil to
dilate. A sympathetically denervated pupil (such as is present in Horner syndrome) dilates poorly
to cocaine, regardless of the level of the sympathetic interruption, because of the absence of
endogenous norepinephrine in the synapse.

For optimal accuracy, test results should be evaluated 30 minutes or longer after cocaine is
administered. The maximal response is seen 40-60 minutes after instillation of the drops.
Postcocaine anisocoria greater than 0.8 mm is sufficient to diagnose Horner syndrome.

The disadvantages of the topical cocaine test are as follows:

The drops are difficult to obtain because they must be made at a compounding pharmacy
The drops are relatively expensive
The test can yield equivocal results
Cocaine metabolites may be detected in urine

Topical apraclonidine test

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The topical apraclonidine test is a practical and reliable alternative to the topical cocaine test; it
is readily available and adequately sensitive (87%) and is currently the test of choice. [22, 23, 24]

Apraclonidine is an ocular hypotensive agent that acts as a weak alpha1-agonist and a strong
alpha2-agonist. [25, 22, 21, 26] Typically given in a 0.5% or 1% solution, it has little to no effect on
a normal pupil but has a mydriatic effect on an abnormal pupil.

In Horner syndrome, upregulation of alpha1-receptors increases apraclonidine sensitivity and

causes denervation supersensitivity of the iris dilator muscle. The denervation supersensitivity
results in pupillary dilatation and lid elevation on the abnormal side but no response or mild
miosis on the normal side from alpha2-activity after apraclonidine administration. Reversal of
anisocoria occurs after bilateral instillation of apraclonidine.

In acute cases, false-negative test results may occur because the alpha1-receptor upregulation
on which the effect of apraclonidine depends may take 5-8 days. [27, 28] Accordingly, a negative
apraclonidine test result, especially in acute settings, does not exclude Horner syndrome. In
such cases, a cocaine test should be performed to exclude Horner syndrome.

Apraclonidine 0.5% or 1% may cause lethargy, bradycardia, and respiratory depression in

infants younger than 6 months as a consequence of the immaturity of the blood-brain barrier. [29]

Topical hydroxyamphetamine test

The localization of a lesion causing Horner syndrome may be aided by the use of the topical
hydroxyamphetamine test. Hydroxyamphetamine stimulates the release of stored endogenous
norepinephrine from the postganglionic axon terminals into the neuromuscular junction at the iris
dilator muscles. This test may distinguish a postganglionic third-order neuron lesion from a
presynaptic second-order or first-order neuron lesion.

To perform the test, 2 drops of 1% hydroxyamphetamine solution are instilled into each eye. A
period of 24-48 hours must be allowed to elapse between the cocaine test and the
hydroxyamphetamine test because cocaine has the ability to inhibit the uptake of
hydroxyamphetamine into the presynaptic vesicles, thereby reducing the accuracy of the latter
test.

Hydroxyamphetamine drops instilled into an eye with Horner syndrome with intact
postganglionic fibers (ie, first- or second-order neuron lesions) dilate the affected pupil to an
equal or greater extent than they do the normal pupil. However, hydroxyamphetamine drops
instilled into an eye with Horner syndrome with damaged postganglionic fibers (ie, third-order
neuron lesions) do not dilate the affected pupil as well as they do the normal pupil.

Treatment & Management

In general, appropriate treatment of Horner syndrome depends on the underlying cause. The
goal of treatment is to eradicate the underlying disease process. In many cases, however, no
effective treatment is known. Prompt recognition of the syndrome and expedient referral to
appropriate specialists are vital.

Whether surgical care is indicated and what type is appropriate depend on the particular cause

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of Horner syndrome. Potential surgical interventions include neurosurgical care for aneurysm-
related Horner syndrome and vascular surgical care for causative conditions such as carotid
artery dissection or aneurysm.

For optimal management of the underlying cause, the following specialist consultations may be
required:

Pulmonology
Internal medicine
Neurology or neuro-ophthalmology
Interventional radiology (in cases of suspected carotid artery dissection)
Surgery or oncology (as warranted by the particular etiology)
Neurosurgery (in cases of suspected aneurysm)

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Contributor Information and Disclosures

Author

Christopher M Bardorf, MD, MS Ophthalmologist, Children's Eye Physicians

Christopher M Bardorf, MD, MS is a member of the following medical societies: American

Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Gregory Van Stavern, MD Attending Physician, Department of Ophthalmology and Neurology,

Washington University School of Medicine

Gregory Van Stavern, MD is a member of the following medical societies: American Academy of
Neurology, North American Neuro-Ophthalmology Society

Disclosure: Nothing to disclose.

Enrique Garcia-Valenzuela, MD, PhD Clinical Assistant Professor, Department of

Ophthalmology, University of Illinois Eye and Ear Infirmary; Consulting Staff, Vitreo-Retinal

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Horner Syndrome: Overview, Anatomy, Pathophysiology 7/19/17, 6:45 AM

Surgery, Midwest Retina Consultants, SC, Parkside Center

Enrique Garcia-Valenzuela, MD, PhD is a member of the following medical societies: American
Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American
Society of Retina Specialists, Retina Society, Society for Neuroscience

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska

Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

J James Rowsey, MD Former Director of Corneal Services, St Luke's Cataract and Laser
Institute

J James Rowsey, MD is a member of the following medical societies: American Academy of

Ophthalmology, American Association for the Advancement of Science, American Medical
Association, Association for Research in Vision and Ophthalmology, Florida Medical
Association, Sigma Xi, Southern Medical Association, Pan-American Association of
Ophthalmology

Disclosure: Nothing to disclose.

Chief Editor

Edsel Ing, MD, MPH, FRCSC Associate Professor, Department of Ophthalmology and Vision
Sciences, University of Toronto Faculty of Medicine; Active Staff, Michael Garron Hospital
(Toronto East Health Network); Consulting Staff, Hospital for Sick Children and Sunnybrook
Hospital, Canada

Edsel Ing, MD, MPH, FRCSC is a member of the following medical societies: American
Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus,
American Society of Ophthalmic Plastic and Reconstructive Surgery, Canadian Medical
Association, Canadian Ophthalmological Society, Canadian Society of Oculoplastic Surgery,
Chinese Canadian Medical Society, European Society of Ophthalmic Plastic and Reconstructive
Surgery, North American Neuro-Ophthalmology Society, Ontario Medical Association, Royal
College of Physicians and Surgeons of Canada, Statistical Society of Canada

Disclosure: Nothing to disclose.

Additional Contributors

Gerhard W Cibis, MD Clinical Professor, Director of Pediatric Ophthalmology Service,

Department of Ophthalmology, University of Kansas School of Medicine

Gerhard W Cibis, MD is a member of the following medical societies: American Academy of

Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, American
Ophthalmological Society

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Horner Syndrome: Overview, Anatomy, Pathophysiology 7/19/17, 6:45 AM

Disclosure: Nothing to disclose.

Acknowledgements

Gerhard W Cibis, MD Clinical Professor, Director of Pediatric Ophthalmology Service,

Department of Ophthalmology, University of Kansas School of Medicine

Gerhard W Cibis, MD is a member of the following medical societies: American Academy of

Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, and
American Ophthalmological Society

Disclosure: Nothing to disclose.

Jules E Harris, MD Clinical Professor of Medicine, Section of Hematology/Oncology, University

of Arizona College of Medicine, Arizona Cancer Center

Jules E Harris, MD is a member of the following medical societies: American Association for
Cancer Research, American Association for the Advancement of Science, American Association
of Immunologists, American Society of Hematology, and Central Society for Clinical Research

Disclosure: GlobeImmune Salary Consulting

Malvinder S Parmar, MB, MS, FRCP(C), FACP Assistant Professor (VPT), Faculty of Medicine,
University of Ottawa Faculty of Medicine; Associate Professor, Department of Internal Medicine,
Northern Ontario School of Medicine; Consulting Physician, Timmins and District Hospital,
Ontario, Canada

Malvinder S Parmar, MB, MS, FRCP(C), FACP is a member of the following medical societies:
American College of Physicians, American Society of Nephrology, Canadian Medical
Association, Ontario Medical Association, and Royal College of Physicians and Surgeons of
Canada

Disclosure: Nothing to disclose.

J James Rowsey, MD Former Director of Corneal Services, St Luke's Cataract and Laser
Institute

J James Rowsey, MD is a member of the following medical societies: American Academy of

Ophthalmology, American Association for the Advancement of Science, American Medical
Association, Association for Research in Vision and Ophthalmology, Florida Medical
Association, Pan-American Association of Ophthalmology, Sigma Xi, and Southern Medical
Association

Disclosure: Nothing to disclose.

Philip Schulman, MD Chief, Medical Oncology, Department of Medicine, Memorial Sloan-

Kettering Cancer Center; Clinical Professor, Department of Medicine, New York University
School of Medicine

Philip Schulman, MD is a member of the following medical societies: American Association for
Cancer Research, American College of Physicians, American Society of Hematology, and

http://emedicine.medscape.com/article/1220091-overview Page 13 of 14
Horner Syndrome: Overview, Anatomy, Pathophysiology 7/19/17, 6:45 AM

Medical Society of the State of New York

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska

Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

http://emedicine.medscape.com/article/1220091-overview Page 14 of 14